The term HTLV (human T-cell leukemia/lymphoma virus) denotes an extended family of retroviruses. There are currently three known members of this family (HTLV-I, HTLV-II, and HTLV-III). The most recently discovered member of the HTLV family (HTLV-III) is thought to be the etiologic agent of acquired immunodeficiency syndrome (AIDS), and it has several immunologic and biochemical features in common with the other viruses. While it is well known that some HTLV viruses can infect and transform T cells, the functional changes that occur in normal T cells that are specifically reactive for a common soluble antigen (for example, tetanus toxoid) are not known. The purpose of the current project was to characterize the functional consequences of HTLV infection in normal human T-cell clones with specificity for soluble tetanus toxoid (and purified protein derivative) using the first and most extensively studied member of the family (HTLV-I) as a prototype. The results indicate that HTLV-I can transform antigen-specific T cells. One unprecedented consequence of HTLV infection in such cells is the loss of the normal T-cell requirement for accessory cell presentation in the activation of an in vitro proliferative response to soluble antigen. Such infected T-cell clones appear capable of binding soluble antigen directly - and colonies of such immune - but infected T-cell clones specifically contract upon exposure to antigen.